Evaluation of 2-deoxy-glucose and glucose absorption in glioblastoma under normal and low oxygen conditions

One of the metabolic signatures of cancer is the overproduction of lactate from glucose during glycolysis. Cancer cells use lactate to sustain the tumor microenvironment and facilitate cancer growth. Previous studies have demonstrated 2-deoxy-glucose (2-DG) is a competitive inhibitor which binds onto glucose transmembrane proteins and prevents cancer growth via limiting hexokinase phosphorylation, preventing glycolysis through stopping production of glucose-6-phosphate (G6P). However, in glioblastoma, it is relatively unknown whether 2-DG uptake among glucose transmembrane proteins is selective when glucose is present under different oxygen levels. In this study, we supplement biological assays testing glucose transmembrane protein expression as it relates to lactate production and cell viability under normal oxygen (i.e., 20% O₂) and low oxygen (i.e., 2% O₂) exposure with a variety of nuclear magnetic resonance (NMR) analysis to better understand the relationship between transmembrane protein activity in different oxygen environments and 2-DG absorption during glioblastoma cell proliferation.